Fu T, Liu G
Department of Pharmacology, Chinese Academy of Medical Sciences, Beijing.
Biomed Environ Sci. 1992 Sep;5(3):185-94.
The protective effect of biphenyl dimethyl dicarboxylate (DDB) on chemically induced damages was studied in isolated suspended rat hepatocytes. The experimental results showed that DDB (200 micrograms/10(6) cells) efficiently protected the hepatocytes against carbon tetrachloride (CCl4 10 mmol.L-1) and D-galactosamine (1 mmol.L-1) induced damages. Membranal lipid peroxidation (malondialdehyde, MDA formation) and glutamic pyruvic transaminase (GPT) release from the hepatocytes were markedly decreased. The damage of the cell surfaces of the hepatocytes were also reduced as seen under a scanning electron microscope (SEM). Pretreatment with DDB (300 mg.kg-1) orally ameliorated the reduction of liver glycogen and blood glucose caused by ip injection of D-galactosamine (800 mg.kg-1) in mice. When normal rats were given DDB 300 mg.kg-1 once daily for 10 d, the free ribosomal protein and RNA in the liver increased significantly. These results indicate that DDB is of beneficial effects on both damaged and normal hepatocytes.
在离体悬浮的大鼠肝细胞中研究了联苯双酯（DDB）对化学诱导损伤的保护作用。实验结果表明，DDB（200微克/10⁶个细胞）能有效保护肝细胞免受四氯化碳（CCl₄ 10毫摩尔/升）和D-半乳糖胺（1毫摩尔/升）诱导的损伤。肝细胞的膜脂质过氧化（丙二醛，MDA形成）和谷丙转氨酶（GPT）释放明显减少。扫描电子显微镜（SEM）观察显示，肝细胞表面的损伤也有所减轻。预先口服给予DDB（300毫克/千克）可改善腹腔注射D-半乳糖胺（800毫克/千克）所致小鼠肝糖原和血糖的降低。正常大鼠每天给予DDB 300毫克/千克，连续10天，肝脏中的游离核糖体蛋白和RNA显著增加。这些结果表明，DDB对受损和正常肝细胞均有有益作用。
